A patient with cirrhosis and ascites has marked secondary hyperaldosteronism yet develops only mild hypoalbuminemia-related edema and no overt peripheral edema for months. The relative protection from progressive edema despite persistently high aldosterone is best explained by:
- A An increase in ANP and pressure natriuresis that offsets sodium retention once extracellular volume expands ✓
- B Downregulation of mineralocorticoid receptors in the distal nephron
- C Conversion of aldosterone to inactive metabolites by hepatic 11-beta-hydroxysteroid dehydrogenase
- D Suppression of angiotensin II by the expanded plasma volume overriding the cirrhotic stimulus
Correct answer: A. An increase in ANP and pressure natriuresis that offsets sodium retention once extracellular volume expands
Explanation
Aldosterone escape occurs in secondary hyperaldosteronism with edema: once extracellular volume expands sufficiently, atrial natriuretic peptide release, increased arterial pressure, and pressure natriuresis promote sodium excretion that counterbalances ongoing mineralocorticoid action. This is why patients with heart failure or cirrhosis do not develop continuously expanding edema despite very high aldosterone. Receptor downregulation (B) is not the accepted mechanism, and 11-beta-HSD2 inactivates cortisol, not aldosterone, in the kidney, eliminating C.
Reference: Ganong Review of Medical Physiology, 26th ed.
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